Severe cognitive deficits are a frequent outcome of both neurodegenerative and neurodevelopmental disorders. In the attempt to define new clinical biomarkers, current research trends aim at the identification of common molecular features in these pathologies rather than searching for differences. Brain-derived neurotrophic factor (BDNF) has attracted great interest as possible biomarker because of its key role in synaptic remodeling during cognitive processes. BDNF undergoes proteolytic processing and studies in animal models have highlighted that different forms of learning and memory require either the proBDNF precursor or the mature BDNF form. Significantly, an altered expression of BDNF forms was found in postmortem brains and serum from patients with schizophrenia, Alzheimer’s disease and mood disorders. Based on these studies, this review puts forward the hypothesis that abnormalities in proBDNF or mBDNF biosynthesis may correspond to different cognitive dysfunctions in these brain diseases, while the role of truncated BDNF remains unknown.

Is Altered BDNF Biosynthesis a General Feature in Patients with Cognitive Dysfunctions?

CARLINO, DAVIDE;DE VANNA, MAURIZIO;TONGIORGI, Enrico
2013-01-01

Abstract

Severe cognitive deficits are a frequent outcome of both neurodegenerative and neurodevelopmental disorders. In the attempt to define new clinical biomarkers, current research trends aim at the identification of common molecular features in these pathologies rather than searching for differences. Brain-derived neurotrophic factor (BDNF) has attracted great interest as possible biomarker because of its key role in synaptic remodeling during cognitive processes. BDNF undergoes proteolytic processing and studies in animal models have highlighted that different forms of learning and memory require either the proBDNF precursor or the mature BDNF form. Significantly, an altered expression of BDNF forms was found in postmortem brains and serum from patients with schizophrenia, Alzheimer’s disease and mood disorders. Based on these studies, this review puts forward the hypothesis that abnormalities in proBDNF or mBDNF biosynthesis may correspond to different cognitive dysfunctions in these brain diseases, while the role of truncated BDNF remains unknown.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11368/2691398
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